Dysphagia is difficulty swallowing that can affect any part of the swallowing pathway from the mouth to the stomach. It is a common complaint seen in ENT clinics. Causes include congenital issues, trauma, infections, inflammation, motility disorders, neurological problems, tumors, and other miscellaneous conditions. Evaluation involves history, examination, blood tests, imaging like barium swallow and endoscopy, and specialized tests like manometry and pH monitoring. Treatment depends on the underlying cause.

1. Dysphagia
Dr.muhanned Alali
S.H.O

2. Definition
Dysphagia
is defined as having difficulty in swallowing which
may affect any part of the swallowing pathway from
the mouth to the stomach.

3. Approximately half of all patients with dysphagia are
seen in ear, nose and throat (ENT) clinics. The
otolaryngologist should know how to diagnose the
cause of the condition and decide which patients to
treat and which patients to refer either to a
gastroenterologist, a neurologist or an oesophageal
surgeon

4. Patients complain that food or liquids are no longer
being swallowed easily and that there is a sensation
of food sticking. Patients will often try to localize the
level of this sensation

5. Physiology of swallowing
1.oral phase
A .mastication
B .addition & mixing of saliva
C .control of bolus (tongue
,lips,buccinator,palat)
D .selection & verification of safty of bolus
(volum,taste,fishbones,etc)

6.  The oral phase is under voluntary control and
ends when the bolus is passed against the
faucial arches to precipitate the involuntary
pharyngeal phase

7.  2. pharyngeal phase
Move the bolus quickly (<1 s) past the closed
glottis and through uos into the esophgus
A . Nasopharyngeal closure with palate
elevation (levator,tensor veli p.) & contraction of
superior con.
B . Cessation of respiration
C . Glottic closur
D . Bolus propulsion

8.  Via tongue base elevation and contraction of
pharyngeal constrictors
E . Laryngeal elevation & pharyngeal shortening
protection of laryngeal vestibule,epiglottic
rotation,and active diltation of cricoph. Sphinctor
F . Epiglottic rotation
Active due to laryngeal elevation
Passive due to pressure bolus
G . Relaxation of cricoph. m

9. 3. Esophageal phase (3-6s)
Nerves of swallowing
A .sensory receptors – softpalate ,tongue
base,pillars and post.ph.wall
B .central ganglion ( V-gasserian , IX– sup.&
inf.((petrosal gang.)) ,X-inf.(jugular) & sup.(nodose)
gang.
C . Efferents
V- teeth,jaw,masticators,& buccinator
V.X- palate

10. VII- lips and facial mm.
IX- pharynx
X- pharynx,larynx,and esophagus
XII- tongue

11. assesment
 Types
 Oropharyngeal and esophageal
 Acute and chronic
 Mural,intramural & extramural

12. oropharyngeal
dysphagia
 difficulty in preparing
 transporting the food bolus through the oral cavity
 initiating the swallow
 associated with aspiration or nasopharyngeal
regurgitation

13. oesophageal
dysphagia
patients complain of food sticking in their lower
throat, neck, retrosternal region or epigastrium

14.  age
Children tend to swallow foreign bodies or have
congenital problems
In middle-aged patients, a cancer or neurological disease
should be excluded though morecommonly they tend to
suffer with reflux oesophagitis, hiatus hernia, anaemia,
achalasia and the globus syndrom
In the elderly, cancer of the swallowing pathway is
much more likely and must be excluded, but other
common causes are stricture formation from longstanding
reflux, pharyngeal pouch, motility disorders associated
with ageing and neurological disorders

15.  onset, duration,
 progression and severity of the symptoms, as
well as the
 types of food that give problems an
 any alleviating factors such as antacids

16. associated
symptoms
 Regurgitation
 Early__bolus obst or tum
 Late---pharyngealpouch.
 Odynophagia
 Infection of upper GIT
 Oesophagitis
 tumor

17.  Hoersness
 Tumor 2ways
 Post laryngeal oedema(reflux)
 Bovin cough(v.c immo
 Otalgia
 Coughing after feeing—aspiration(lary.
Incomp ,hypopharyn dysf
Rln by tum

18. Medical and surgical HX

19. head and neck examination with careful
inspection of the oral cavity, dentition and
oropharynx and to include indirect laryngoscopy
and or nasolaryngoscopy to
inspect the rest of the pharynx and larynx and to
exclude `pooling of saliva

20.  Cranial nerve function is assessed to
look for loss of tongue movement, wasting and
fasciculation,
 loss of gag and cough reflexes, loss of
pharyngeal
and laryngeal sensation, the presence of
hoarseness
 and loss of vocal cord mobility

21. .. The neck is examined
for lymph nodes and other neck masses, thyroid
enlargement, loss of laryngeal crepitus and the
integrity of the laryngeal cartilages
. General physical and neurology
examinations should look for evidence of malnutrition,
weight loss, chest disease, epigastric tenderness and
abdominal swellings, loss of coordination,
fasciculation and tremor.

22. investigation
A full blood count and indices should be obtained in all
patients to exclude anaemia as a cause or effect of the
dysphagia.
(ESR) or C reactive protein may be raised in malignancy or
chronic inflammatory processes.
Liver and renal function tests
together with serum calcium levels should be acquired
when nutrition is impaired or metastases are suspected.
Thyroid function tests are indicated if dysphagia is caused
by a goitre or thyroid malignancy.
Creatine kinase levels may be elevated in myopathies

23. Barium swallow
All patients with dysphagia should have a
barium swallow if the cause is not obvious after
an ENT
 the test focusses on the oesophagus
is poor for picking up pharyngeal
disease,especially in the postcricoid
 Barium swallow may confirm reflux, but it is
not a very sensitive investigation as it fails to
pick up 40 percent

24. Barium study
 It is useful for diagnosing a
 pharyngeal pouch,
 stricture,
 hiatus hernia
 or an obstructing esophageal lesion

25. Contarind.
 Perforation
 Aspiration

28. CXR
 All pts with true dysphagia
 Looks for sign of aspiration ,
infection,metastasis
CT
 For tracking tum. And metastasis

29. MRI
 Neorological cause
 Lesions around FM .BS
 Vascular abormality

30. Direct pharyngoscopy
&rigid endoscopy under GA
 For pharynx and upper oesophagus esp.
when barium swallow was normal
 Most reliable for postcricoid

31. Flexible upper GI
oesophagioscopy under GA
By gastroenterologist or esophageal surgeon
To visualize,asses,stage and take BX
 Oesophagitis,barret`s esophagus and tumor
 Poor in pharyngeal diseases because
 Passed through rapidly
 Unable to examine pyriform sinus adequately

32. Barium videofloroscopic swallow
study
VFSS
 Gold standard for swallowing mechanism
 Mainly oral and pharyngeal phase
 Evaluate ; transit time,pooling,aspiration
 Motor funtion&symetry of swallowing pathway

33. Fibrooptic endoscopic evaltuaion
of swallowing (F.E.E.S)
 Pooling in hypopharynx
 Endolaryngeal sensation
 Aspiration
 Useful in
 Neurological
 Frail
 Postsurgical
 All phases can`t assesed directly
 Cricopharynx and eosophagus not visualized

34. manometry
 Measure oesophageal pressure at rest and
swallowing to diagnose motility disoreder
 Useful in atypical chestpain and unexplained
cause of dysphagia
 Achalsia,DES,nutcrcker oeasophagus and
scleroderma

35. 24 hr ambulatory esophageal PH
monitoring
 Most accurate for esophageal reflux dz
 Standard investigation was normal in pt with
typical chestpain
 Pt with atypical symptom as in
chestpain,glopus,hoersness,& recurrent chest
infection

36. Comparison oF. 􀄐i􀄐fluoroscopy with FEES and
manometry
Feature F.E.E.S VFL MANOMETRY
Hazard Cross infection radiation Cross infection
Versa til ity portable X-ray dep. portable
Oral stage indirect yes no
Pharyngeal stage yes yes pressure
Oesophagal stage Not consistently
seen
Can be
observed
pressure
Aspiration/penetration yes yes no
Pharyngeal sensation yes Only inferred no
Range of boluses all Rad io-opaq ue contrasts a
Iter
viscosity, texture and taste of
food/drink
yes
Biofeedback good good limited

37. Causes of dysphagia
 Congenital:
- choanal atresia;
- cleft lip and palate;
- laryngomalacia;
- unilateral vocal cord paralysis;
- laryngeal cleft;
- tracheooesophageal fistula and oesophageal
atresia;
- vascular rings

38.  Acquired:
- traumatic:
• accidental and iatrogenic;
• blunt trauma, penetrating injuries and
compression effects;
• direct injury and cranial nerve damage;
• head injury.

39.  infections:
• acute pharyngitis, tonsillitis, quinsy;
• glandular fever;
• acute supraglottitis;
• herpetic, fungal, cytomegalovirus mucosal
lesions;
• candidiasis;
• tuberculosis;
• submandibular, parapharyngeal and
retropharyngeal abscesses.

40.  inflammatory:
• gastrooesophageal reflux disease ± stricture
formation;
• Patterson Brown-Kelly or Plummer-Vincent
syndrom
• systemic autoimmune disorders: scleroderma
and 'CREST' syndrome; systemic lupus
erythematosus; dermatomyositis; mixed
connective tissue disease; benign pemphigoid
and epidermolysis bullosa; primary and
secondary Sjogren's diseases; rheumatoid
arthritis; Crohn's disease; sarcoid.

41.  oesophageal motility disorders:
• achalasia;
• diffuse oesophageal spasm;
• 'nutcracker' oesophagus
 neoplastic:
• benign tumours of the oral cavity, pharynx
and oesophagus;
• malignant tumours of the oral cavity,
pharynx and oesophagus;
• nasopharyngeal carcinoma;
• skull base tumours;
• leukaemias and lymphomas;
• enlarged mediastinal lymph nodes

42.  neurological:
• cerebrovascular accidents (stroke);
• isolated recurrent laryngeal nerve palsy;
• Parkinson's disease;
• multiple sclerosis;
• myasthenia gravis;
II motor neurone disease

43.  drug-induced:
• drugs causing oesophagtis;
• inhibitory drug side effects;
• excitatory drug side effects;
II drug complications
 - ageing:
• presbydysphagi

44.  miscellaneous:
• foreign bodies in the pharynx and
oesophagus;
II caustic stricture;
• pharyngeal pouch;
• globus pharyngeus;
• patients with tracheostomy;
• thyroid disease.

45. Congenital
Choanal atresia
 Partial feeding difficulties as the neonate is an
obligate nasal breather and unable to suckle adequately
 Complete respiratory distress
Cleft lip and/or palat
 inadequate lip seal
 inability to seal off the nasopharynx and nasal
cavity

46. Unilateral vocal cord paralysis
 swallowing difficulties,
 Hoarseness
 Aspiration
Laryngomalacia
Laryngeal clefts
Tracheooesophageal fistula
Vascular rings

47. Traumatic
Neck injuries
 Directly disrupt the swallowing
 Indirectly affecting the cranial nerves IX to X
Head injuries
paresis, paralysis or loss of coordination
of the swallowing mechanism which may not
become apparent until the patient resumes
consciousness, starts
feeding again and aspiration results

48. Infections
 Acute pharyngitis and tonsillitis
 Glandular fever
 Acute supraglottitis
 Herpetic, fungal or cytomegalovirus mucosal infections
 Oral candidiasis
candida affecting the hypopharynx and oesophagus may not be
obvious to the clinician
The barium swallow demonstrates a characteristic 'shaggy' mucosal
appearance that may make endoscopy unnecessary for some patients

49. Tuberculosis
 mucosal lesion
 enlarged lymph nodes
Abscesses of the head and neck space
 peritonsillar abscesses followed by submandibular and
parapharyngeal abscesses
 Retropharyngeal abscesses, which are rare in adults,
are more common in children.

50. Inflammatory
Gastrooesophageal reflux disease
(GORD)
 tightness in the lower neck, constant
throat clearing, retrosternal discomfort and
hoarseness
 gradually increasing dysphagia
when the acid reflux is associated with stricture
formation

51. Patterson Brown-Kelly or Plummer-Vincent
syndrome
 The dysphagia is due to hyperkeratinization with web
formation in the postcricoid region
 can be seen on barium swallow,
but may not always be found at rigid endoscopy
Systemic autoimmune disorders
Steroids and immunosuppressive drugs does not
usually improve the dysphagia.

52. Scleroderma and 'CREST' syndrome
 Affect the lower oesophagus
 Poor peristalsis
 severe gastrooesophageal reflux
 Stricture formation
 Barrett's oesophagus.
Systemic lupus erythematosus (SLE)
 dysphagia tends to be mild.

53. Dermatomyositis
 secondary to hypopharyngeal and upper oesophageal
involvement
Benign pemphigoid and epidermolysis bullosa
 good response to steroids and dilatation
Sjogren's diseases
Rheumatoid arthritis
Sarcoid
 by involved lymph nodes

54. Oesophageal motility disorder
Achalasia (cardiospasm)
 Manometry(in early disease when the classic
barium appearance has not yet developed)
 failure of relaxation of the LOS
 absence of oesophageal peristalsis
 raised resting pressure in the oesophagus

55. Diffuse oesophageal spasm
Manometry shows
 repetitive nonperistaltic, multipeaked contractions of high
amplitude of the body of the oesophagus with
intermittent normal peristalsis
 incomplete lower oesophageal sphincter relaxation.
 Barium swallow
shows a characteristic nonpropulsive peristaltic wave

56. Nutcracker oesophagus
Manometry shows
normal peristaltic waves of high amplitude in the distal
oesophagus.

57. Neoplastic
In the oral cavity
 95% SCC
 Lump or ulcer
 Dysphagia by tongue fixation
In the oropharynx
 usually ulcerative
 The patient usually presents with a sorethroat, referred
otalgia or dysphagia
 should be visible clinicly

58. In the hypopharynx
 60% in the pyriformfossa.
 Small tumors and tumors of the postcricoid region
or the cervical oesophagus can be more difficult to
diagnose
 The ENT examination and barium swallow may be
normal
 The patient may only complain of a feeling of 'something
in the throat', a crumb being stuck or have had any
episode of food stick

59.  but if those symptoms are either
constant or persistent, especially when associated with
arytenoid oedema or pooling of saliva on examination, a
direct pharyngoscopy and oesophagoscopy is mandatory
In the oesophagus
Dysphagia of short duration in an elderly male
who smokes and drinks and which progresses from solids
to liquids is classical

60.  In all cases of pharyngeal and oesophageal malignancy,
the diagnosis is confirmed by biopsy performed under
general anaesthesia in order to assess and stage the
tumor
Nasopharyngeal carcinomas
cranial nerve palsies from skull base invasion
resulting in speech and swallowing problems and
hoarseness

61. Skull base tumours, such as craniopharyngomas and
chordomas
 compression of the parapharyngeal space
 invasion of the cranial nerve
Leukaemias and lymphomas
 oesophageal wall infiltration

62. Neurological
Cerebrovascular accident or stroke
 affecting the cortex or the corticobulbar tracts
(pseudobulbar palsy)
 by affecting the bulbar nerve nuclei (bulbar palsy)
 delayed triggering of the swallowing reflex
 cricopharyngeal dysfunction
 Reduced tongue control and pharyngeal contraction
and cough
 Loss of pharyngeal sensation--- ASPIRATION

63. Isolated recurrent laryngeal nerve palsy
 Decreased pharyngeal gradient pressures
 Decreased glottic closure pressures
 inferior constrictor and cricopharyngeus muscle
dysfunction
Parkinson's disease
 The oral phase of the swallow is affected by rigidity of
the tongue musculatur
 pharyngeal phase by delayed contraction of the
pharyngeal muscle

64. Multiple sclerosis
 Reduced pharyngeal Peristalsis
 Delayed swallowing reflex
 However, the demyelinating lesions can
occur in a single cranial nerve or cause a general
dysfunction of all three phases of deglutition

65. Myasthenia gravis
 Bulbar muscle weakness is the cause of the dysphagia
 slow and weak tongue Movements
 fatigue of swallowing
 food residue in the Oropharynx
 laryngeal penetration and aspiration

66. Motor neurone disease (amyotrophic lateral
sclerosis)
 progressive disease of the corticobulbar and
corticospinal tracts
 mainly the oral and oropharyngeal stage of swallowing
together with dysarthria and anarthria

67. Drug-induced
 Drugs can cause dysphagia directly by causing
oesophagitis
 or as part of their pharmacological action
 or normal side effects

68. Ageing (Presbydysphia)
 The oral phase
 loss of teeth and tongue connective tissue
 reduced strength of mastication
 weakness of the velopharyngeal reflexes.
 The pharyngeal phase
 Decreased elevation of the larynx
 Prolongation of the pharyngeal transit time

69. Ageing (Presbydysphia)
 In the oesophageal stage
 prolongation of the upper oesophageal sphincter relaxation
time and the oesophageal transit time

70. Miscellaneous causes of
dysphagia
 FOREIGN BODIES IN THE PHARYNX
 FOREIGN BODIES IN THE OESOPHAGUS
 CAUSTIC STRICTURE
 PHARYNGEAL POUCH
 Manometric studies suggest that it is associated with high
intrapharyngeal pressures with a high resting tone in cricopharyngeus
that is slow to relax
 GLOBUS PHARYNGEUS
 constant feeling of a lump in the throat' which is worse on
swallowing saliva, but not with fluids or food.

71.  associated with gastrooesophageal reflux with or
without oesophagitis
 increased upper oesophageal sphincter pressures and it
has been postulated that this is secondary to the
gastrooesophageal reflux

72. Compensatory strategies
POSTURAL TECHNIQUES
reducing or eliminating aspiration in 75-80 percent of patients
Head back (utilizes gravity to clear oral cavity). This is used to
improve inefficient oral transit of the bolus.
Chin down (widens valleculae to prevent the bolus
from entering the airway; reduces risk of aspiration).
This is used
 if the triggering of the swallow reflex is delayed;
 also it is used to clear residue from the valleculae,
 if there is evidence of reduced posterior movement of the tongue
base

73.  Head rotation towards the damaged side (directs the
bolus down the stronger side). This is used with patients
where a unilateral vocal fold palsy or hemilaryngectomy
results in aspiration during the swallow.
Lying down on one side (eliminates the effect of
gravity on the pharyngeal residue). This is used with
patients where there is demonstrated reduced
pharyngeal contraction, where residue is seen
throughout the pharynx

74. Head tilt towards the stronger side (eliminates
the damaged side of the pharynx from the direction of
bolus transit)
This is used in cases of unilateral oral and pharyngeal
palsy on the same side (illustrated by residue on the same
side of the mouth and pharynx

75. Head rotated (pulls the cricoid cartilage away
from the posterior pharyngeal wall, reducing pressure
on the cricopharyngeal sphincter).
This posture is used where cricopharyngeal dysfunction is
demonstrated by visible residue in the pyriform sinuses

76.  CHANGES VOLUME/SPEED OF FOOD
PRESENTATION
Where a patient has a delay in triggering the
pharyngeal stage swallow, or has weak pharyngeal
musculature such that the bolus takes time to clear,
each swallow may take two or three attempts per
bolus to clear. If eating too quickly, food can rapidly
build up in the
pharynx and aspiration may ensue.

77.  TECHNIQUES TO IMPROVE ORAL SENSORY
AWARENESS
delayed onset of the swallow (either at the
oral or the pharyngeal stage).
 increasing downward pressure of the spoon
against the tongue when food is presented
 presenting a sour bolus (lemon flavoured barium)
 presenting a cold bolus
 presenting a bolus needing chewing
 presenting a larger volume of bolus

78.  self-feeding from hand to mouth
 Techniques that enhance sensory input
Changing taste, temperature and volume of the bolus
presented, may assist patients who have a swallow
apraxia

79. TECHNIQUES TO IMPROVE SPEED
OF TRIGGERING THE
PHARYNGEAL SWALLOW
 Thermo-tactile stimulation
using a paediatric laryngeal mirror (size 00) that has been held
in crushed ice to chill it. The mirror is then firmly rubbed along
the anterior faucial arches, four or five times, before presenting
the bolus to be swallowed.
 An exaggerated suck-swallow action
vertical tongue-jaw movements with the lips closed
 facilitates triggering of the swallow
 allows saliva to be taken to the back of the mouth
may help some oral cancer patients who have limited
saliva control

80. DIETARY CHANGES
Patients who present with a delay in triggering the
pharyngeal swallow and/or reduced airway closure are
those most at risk from aspiration of thin fluids and these
patients may not demonstrate improvement when using
compensatory strategies such as postural changes or oral
sensory procedures

81. PROSTHETICS
Typically, prostheses are used when patients
are left with part, or all, of the soft palate ablated and a
defect left in the reconstructed area
 A palatal lift (which lifts the soft palate into a closed
position
 A palate-lowering
necessary for patients who have significant (> 50
percent) tongue resected and/or the remaining tongue is
severely reduced in movement

82. Rehabilitative therapy
 Indirect therapy
used with patients who are deemed unsafe on
oral intake and involves no food or liquid being
Used
(ROM, resistance exercises, chewing
and swallow manoeuvres without food)
swallows their own saliva

83.  Direct therapy
involves the patient being taught to gain control over the
bolus, using small amounts of food or liquid, using
specified swallowing sequences. This is only used when
patients can successfully swallow small amounts with
no aspiration

84. Q ;
the defining lvl between penetration &
aspiration?
Thank you